文献类型： 外文期刊

作者： Xu, Ruze ¹ ; Zheng, Ruizhou ¹ ; Wang, Yali ¹ ; Ma, Rongrong ¹ ; Tong, Guixiang ⁴ ; Wei, Xinxian ⁴ ; Feng, Dongyue ² ; Hu, ¹ ;

作者机构： 1.Shanghai Ocean Univ, Natl Pathogen Collect Ctr Aquat Anim, Shanghai Engn Res Ctr Aquaculture, Natl Demonstrat Ctr Expt Fisheries Sci Educ, Shanghai 201306, Peoples R China

2.Natl Fisheries Tech Extens Ctr, Beijing 100125, Peoples R China

3.Chinese Acad Fishery Sci, East China Sea Fisheries Res Inst, Key Lab East China Sea Fishery Resources Exploita, Minist Agr, Shanghai 200090, Peoples R China

4.Guangxi Acad Fishery Sci, Guangxi Key Lab Aquat Genet Breeding & Hlth Aquac, Nanning 530021, Peoples R China

关键词： Fenvalerate; Sulfide gatifloxacin; Ridomil; Hepatopancreas; Transcriptome; Toxicity mechanism

期刊名称：FISH & SHELLFISH IMMUNOLOGY （ 影响因子：4.581； 五年影响因子：4.851 ）

ISSN： 1050-4648

年卷期： 2021 年 116 卷

页码：

收录情况： SCI

摘要： Most antibiotics, insecticides, and other chemicals used in agricultural and fishery production tend to persist in the environment. Fenvalerate, sulfide gatifloxacin, and ridomil are widely used in aquaculture as antibacterial, antifungal, and antiparasitic drugs; however, their toxicity mechanism remains unclear. Thus, we herein analyzed the effects of these three drugs on the hepatopancreas of Procambarus clarkii at the transcriptome level. Twelve normalized cDNA libraries were constructed using RNA extracted from P. clarkii after treatment with fenvalerate, sulfide gatifloxacin, or ridomil and from an untreated control group, followed by Kyoto Encyclopedia of Genes and Genomes pathway analysis. In the control vs fenvalerate and control vs sulfide gatifloxacin groups, 14 and seven pathways were significantly enriched, respectively. Further, the effects of fenvalerate and sulfide gatifloxacin were similar on the hepatopancreas of P. clarkii. We also found that the expression level of genes encoding senescence marker protein-30 and arylsulfatase A was downregulated in the sulfide gatifloxacin group, indicating that sulfide gatifloxacin accelerated the apoptosis of hepatopancreatocytes. The expression level of major facilitator superfamily domain containing 10 was downregulated, implying that it interferes with the ability of the hepatopancreas to metabolize drugs. Interestingly, we found that Niemann pick type C1 and glucosylceramidase-beta potentially interact with each other, consequently decreasing the antioxidant capacity of P. clarkii hepatopancreas. In the fenvalerate group, the downregulation of the expression level of xanthine dehydrogenase indicated that fenvalerate affected the immune system of P. clarkii; moreover, the upregulation of the expression level of pancreatitis-associated protein-2 and cathepsin C indicated that fenvalerate caused possible inflammatory pathological injury to P. clarkii hepatopancreas. In the ridomil group, no pathway was significantly enriched. In total, 21 genes showed significant differences in all three groups. To conclude, although there appears to be some overlap in the toxicity mechanisms of fenvalerate, sulfide gatifloxacin, and ridomil, further studies are warranted.